The somatic motility theory proposes that the sound signal is amplified by an amplifier protein, called prestin, embedded in the hair cell membrane.
Prestin is powered by voltages within the membrane that are produced by mechanical sound vibrations.
"This motility is also called 'dancing' because when you electrically stimulate an outer hair cell with a sound, the cell body spontaneously elongates and contracts along with the sound. It is very dramatic to see these hair cells 'dance' with the sound," said Jian Zuo, Ph.D., associate member of the St. Jude Department of Development Neurobiology.
In the research, the scientists genetically altered mice to have only subtle alterations in the prestin protein. These alterations only compromised prestin's function as an amplifier but did not otherwise affect the outer hair cell structure or function, the researchers' analysis showed.
"We found that these mice showed exactly the same kinds of hearing deficiency as the previous knockout mice. Therefore, we believe that these experiments eliminate criticism of our earlier experiments with the knockout mice," Zuo said.
The new experiments, Zuo said, thus firmly establish that the "dancing" somatic motility of the outer hair cells is critical to cochlear amplification.
However, he noted, "With this study we still cannot really exclude stereociliary motility from contributing to cochlear amplification, because eliminating somatic motility also reduces ciliary motility. So, it is not possible to totally isolate either form of motility. In fact, we hypothesize that the two mechanisms might work together in different aspects of amplification."
The study is published in the May 8 issue of the journal "Neuron."
Source-ANI
RAS/L